Deep vein thrombosis is one of venous thromboembolism clinical manifestations,but also a serious,potentially dangerous disease.Thrombosis can occur in various parts of the body veins,and deep venous thrombosis is the most common.Even though most patients with DVT have no clinical symptoms or with mild symptoms,but failure to timely appropriate treatment is easy to progress to post thrombotic syndrome,shares bruises,stock white swollen,which can occur in severe pulmonary embolism and cause death.Although clinically in a variety of measures to prevent DVT formation,including physical prevention and drug prevention,but the incidence of deep vein thrombosis remains high,9-36％ after total hip arthroplasty,and 52％ after total knee arthroplasty.DVT is a disease combined with genetic and non-genetic factors,60％ DVT patients have hereditary risk factors.Currently genetic factors on the formation of DVT study find that clotting factor Ⅺ gene polymorphisms is associated with DVT.Coagulation factor Ⅺ (F Ⅺ) is a serine protease synthesized by the liver and plays an important role in the coagulation cascade process such as maintain the amplification process and the intrinsic pathway.Research on correlation between single nucleotide polymorphisms (SNPs) of F Ⅺ locus rs2289252 and rs2036914 and deep vein thrombosis has become popular.This paper reviews the discovery of coagulation F Ⅺ single nucleotide polymorphism associated with DVT,the degree of association between coagulation F Ⅺ single nucleotide polymorphism and the formation of DVT,risk allele on the clotting F Ⅺ single nucleotide polymorphism,clinical trials of coagulation F Ⅺ and the formation of DVT,coagulation F Ⅺ single nucleotide polymorphisms interact with other genetic polymorphisms,etc.Although the single nucleotide polymorphism in DVT formation mechanism is still vague,we believe that further study of single nucleotide polymorphisms associated with DVT will provide new approaches to prevention and treatment of DVT.

This review summarized the biological activities of natural saponins,introduced its action mechanisms,clinical applications and research progresses in cardiovascular system,antitumor,immunological enhancement,blood sugar suppression,contraception,antifugal and insecticide,etc,and prospected its exploitations.

Objective To investigate the regulatory effect of glutamate signaling pathway on filopodia formation in epidermal cells and on melanosome transfer.Methods Epidermal melanocytes and keratinocytes were isolated from human foreskin and subjected to subculture.After two to three passages of subculture,the melanocytes and keratinocytes were cultured alone or in combination with or without the presence of MK801 (an antagonist of N-methyl-D-aspartic acid (NMDA) receptor) of 100 μmol/L,or NMDA (the activator of NMDA receptor) of 100 μmol/L,for 24 hours.The melanocytes irradiated with UVB at 311 nm served as the control.Scanning electron microscopy was used to observe the appearance of filopodia and dendrites of melanocytes and keratinocytes.Melanosome transfer was visualized under confocal laser scanning microscopy after double immunofluorescent staining.Results Although no obvious changes were observed in the number of dendrites in monocultured melanocytes after treatment with MK801 or NMDA for 24 hours,dendrites became thinner at the terminus and longer with a decrease in the number and length of filopodia after MK801 treatment,but thicker and shorter with an increase in the number and length of filopodia after NMDA treatment compared with untreated monocultured melanocytes.In the coculture system,filopodia were observed between the untreated melanocytes and keratinocytes,and the number of filopodia in melanocytes was larger in the side adjacent to keratinocytes than in the opposite side.Compared with the untreated coculture system,the number of both filopodia connecting melanocytes and keratinocytes and filopodia extending from melanocytes to keratinocytes decreased in the coculture system after treatment with MK801 of 100 μmol/L,but increased after treatment with NMDA of 100 μmol/L,for 24 hours.Melanosomes were found in keratinocytes cocultured with melanocytes without treatment,which were decreased in number after 24-hour treatment with MK801 of 100 μmol/L,but increased in number and even present in keratinocytes nonadiacent to melanocytes after 24-hour treatment with NMDA of 100 μmol/L.Conclusion Glutamate signaling pathway may modulate the transfer of melanosomes from melanocytes to keratinocytes via modulating the appearance of melanocyte dendrites and formation of filopodia.

Alzheimer′s disease ( AD) , is a neurodegenerative disorder of the brain that is characterized by loss of memory and cognitive decline.At present, AD etiology remains unclear and there are no effective prevention and treatment measures in clinical practice.Peroxisome proliferator-activated receptorγ( PPARγ) is a ligand-regulated nuclear hormone receptor.Recent studies showed PPARγ-pathway played an important role in the pathogenesis of AD and some PPARγagonists have been proven to be neuroprotective in vitro and in vivo models.This paper reviews the roles of PPARγand related mechanisms in AD, summarizes affecting factors about PPARγpathway.Particularly, the effect of cyanidin-3-O-glucoside ( Cy3G) , one of the anthocyanidin glycoside forms, is a compound of naturally occurring phenolic compounds, suggesting the neuroprotective effect of Cy3G might be used as a potential natural PPARγagonist in the nervous system.

Individual susceptibility to cancer induced by environmental agents may be influenced by polymorphic metabolic genes responsible for the activation or detoxification of carcinogens．The association between genetic polymorphisms in cytochrome P4501A1 (CYP1A1) and lung cancer susceptibility has been extensively studied．The various CYP1A1 alleles exhibit population frequencies that depend on race and ethnicity．An increased risk of lung cancer in Asians was found to be associated with genetic polymorphisms in CYP1A1．However，reports from Caucasians are not consistant，probably suggesting the ethnic-sepecific effect of the polymorphisms in the locus on the cancer．Evidence also exists for the association between levels of carcinogen-DNA adducts or frequency of oncogene and tumor suppressor gene mutations and CYP1A1 polymorphisms．These findings provide a better understanding of the relationship between CYP1A1 and lung cancer susceptibility．

Objective To evaluate the effect of HTK solution on myocardial protection during valve replacement surgery.Methods 42 patients with rheumatic heart disease were randomized to receive 4∶1cold blood (control group,n =21 ) and HTK ( protective gronp,n =21 ) cardioplegic solution during valve replacement.The changes of CO and CI were collected at different time points including pre-operation,postoperative 6 hours,12 hours and 24 hours.Aortic clamping time,the ratio of spontaneous cardiac rhythm recovery and inotropic drugs application were calculated,and mechanical ventilation support time and the incidence of arrhythmia were recorded.Results The measurements of CO and CI showed that there was significant higher level in protective group at postoperative 12 hours and 24 hours [ 12 h:(4.82 ± 0.18 ) L/min vs ( 3.50 ± 0.32 ) L/min,( 3.80 ± 0.48 ) L/( min · m2 ) vs (2.79 ± 0.39) L/( min · m2 ) ;24 h:(4.97±0.45)L/min vs ( 3.81 ±0.19)L/min,(4.22±0.17)L/(min · m2) vs (2.91 ±0.21)L/(min·m2 ),P ＜ 0.05].The clinical parameters including aortic clamping time,incidence of cardiac arrhythmia,inotropic support,duration of mechanical ventilation and length was lower than in control group [ (53.6 ±24.3 ) min vs ( 68.9 ± 26.1 ) min ; ( 1.8 ± 1.3 ) min vs ( 2.3 ± 1.2 ) min ; ( 33 ± 11 ) min vs ( 42 ± 13 ) min ;(10.2±2.1) μg/(kg · min) vs (15.7 ±3.8) μg/(kg · min);(14.6 ±4.8)h vs (20.7 ±5.1)h,P ＜0.05].The auto-beating rate was higher than in control group (90％ vs 67％,P ＜0.05).Conclusions HTK solution is better than classical blood cardioplegia in myocardial protection during valve replacement.

Objective To construct and screen the human immunodeficiency virus-1 (HIV-1) negative regulation factor (Nef) peptide-specific CD4+ T lymphocyte clone.Methods Peripheral blood mononuclear cells (PBMC) from five asymptomatic HIV-1 infected patients were collected and Bulkcultured with Nef end peptides.The CD4 molecule and intracellular interferon (IFN)-gamma of cultured cells were detected by two-color flow cytometry.The Nef end peptide-specific T cell clone was then constructed by limited dilution and confirmed through enzyme linked immunospot assay (ELISPOT).The best grown cells were selected and cultured as the final clone.Results The Nef end peptide-specific-T lymphocyte clone was successfully constructed from PBMC of one HIV-infected patient and confirmed by ELISPOT.The detection of human leukocyte antigen (HLA)-DRB1 type showed that the epitope of this peptide was probably HLA-DRB1 * 0406.Conclusion The Nef end specific-T cell clone is successfully constructed,and a new epitope in the C-terminus of Nef protein and its HLA restriction are identified.

Drugs, Chinese Herbal ; pharmacology ; Embryo Implantation ; drug effects ; Endometrium ; drug effects ; physiology ; Female ; Humans

Objective To identify the clinical characteristic of familial Creutzfeldt-Jakob disease(fCJD) in one pedigree with four cases in two-generation and to investigate its pathogenetic mechanism.Methods The pedigree was investigated in the fCJD kindred,protein capture assay was used to do quantitative analysis of 14-3-3 protein in the cerebrospinal fluid.Types of PrP gene mutation were studied by polymerase chain reaction(PCR) and DNA sequence analysis.Results(1) The onset age during four cases in two-generation was lower than the sporadic CJD and it tended to go down by generations.(2) The 14-3-3 protein level in the index case's cerebrospinal fluid was 125 ng/ml,which was higher than intersection point by 13.9 times.(3) In the index case,inserting mutation in site 231 of PRNP was induced by an adenine insertion between base 788 and 789.(4) No PrP gene mutation was found in the index case's younger brother and daughter.Conclusions The fCJD is identified in the index case,which is caused by inserting mutation in the site 231 of PRNP.There is no significant difference in the clinical manifestations between fCJD and sporadic CJD.However,the onset age of fCJD is lower than the sporadic CJD and patients from the same pedigree die at familiar ages.

Objective To determine the changes in phosphorylation of conventional protein kinase C?(cPKC?)-interacting extracellular signal regulated kinase 1/2(ERK1/2) in the hippocampus of hypoxic preconditioned(HPC) mice.Methods Healthy male BalB/c mice were used to develop "auto-hypoxia"-induced HPC mice and randomly divided into 3 groups as follows: normoxic control(H0),early(H3) and delayed hypoxic preconditioned groups(H6).Co-immunoprecipitation and Western blot were applied to quantitatively analyze the phosphorylation level of cPKC?-interacting ERK1/2 in cytosolic and particulate fractions of hippocampus of HPC mice.ResultsERK1/2 was co-immunoprecipitated by cPKC? in hippocampus of mice.The phosphorylation level of cPKC? interacting ERK1/2 at tyrosine 204 decreased significantly in the hippocampus of H3 and H6 groups as compared with that of the H0 group(P